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Myo-mechanical Analysis of Isolated Skeletal Muscle
Published on: February 23, 2011
Myogenic NOS and endogenous NO production are defective in colon from dystrophic (mdx) mice
F Mulè1, M G Vannucchi, L Corsani
1Dipartimento Farmaco-Biologico, Università della Calabria, 87036 Arcavacata di Rende (CS), Italy. fmule@unipa.it
Abstract:
The aim of the present study was to evaluate whether alterations in the distribution and/or function of nitric oxide synthase (NOS) could be involved in the development of the spontaneous mechanical tone observed in colon from dystrophic (mdx) mice. By recording the intraluminal pressure of isolated colon from normal mice, we showed that N(omega)-nitro- L-arginine methyl ester (L-NAME) increased the tone, even in the presence of tetrodotoxin. The effect was prevented by L-arginine, nifedipine, or Ca(2+)-free solution. In colon from mdx mice, L-NAME was ineffective. Immunohistochemistry revealed that the presence and distribution of neuronal (nNOS), endothelial, and inducible NOS isoforms in smooth muscle cells and neurons of colon from mdx mice were the same as in controls. However, the expression of myogenic nNOS was markedly reduced in mdx mice. We conclude that there is a myogenic NOS in mouse colon that can tonically produce nitric oxide to limit influx of Ca(2+) through L-type voltage-dependent channels and modulate the mechanical tone. This mechanism appears to be defective in mdx mice.
Insights
Altered nitric oxide synthase (NOS) function in dystrophic mice colon impairs myogenic tone. This nitric oxide (NO) production defect limits calcium channel modulation, affecting mechanical tone in mdx mice.
Area of Science:
- Gastroenterology
- Physiology
- Molecular Biology
Background:
- Spontaneous mechanical tone in colon is crucial for gastrointestinal motility.
- Nitric oxide synthase (NOS) plays a role in regulating smooth muscle function.
- Dystrophic (mdx) mice exhibit altered muscle function.
Purpose of the Study:
- To investigate the role of nitric oxide synthase (NOS) alterations in the spontaneous mechanical tone of mouse colon.
- To determine if NOS dysfunction contributes to the observed tone in dystrophic (mdx) mouse colon.
Main Methods:
- Recording intraluminal pressure of isolated mouse colon.
- Utilizing N(omega)-nitro-L-arginine methyl ester (L-NAME) to inhibit NOS activity.
- Employing immunohistochemistry to assess NOS isoform distribution and expression.
- Examining the effects of L-arginine, nifedipine, and Ca(2+)-free solutions.
Main Results:
- In normal mouse colon, L-NAME increased tone, an effect blocked by L-arginine, nifedipine, or Ca(2+)-free solution.
- L-NAME was ineffective in colon from mdx mice, indicating impaired NOS function.
- Immunohistochemistry showed similar distribution of nNOS, eNOS, and iNOS isoforms in mdx and control mice.
- Myogenic nNOS expression was significantly reduced in mdx mouse colon.
Conclusions:
- A myogenic NOS in mouse colon tonically produces nitric oxide (NO).
- This NO production limits Ca(2+) influx via L-type channels, modulating mechanical tone.
- This NO-mediated mechanism for regulating colonic tone is defective in mdx mice.
